Blood oxidative stress markers in non-alcoholic steatohepatitis and how it correlates with diet.
OBJECTIVE
Non-alcoholic fatty liver disease is a common condition that can progress to endstage liver disease. The steatotic liver seems to be particularly susceptible to oxidative stress damage. The aim of this study was to evaluate the redox state in patients with non-alcoholic steatohepatitis (NASH) and its correlation with dietary intake.


METHODS
Plasma concentrations of 4-hydroxynonenal (4-HNE), 8-hydroxydeoxyguanosine (8-OHdG), reduced and oxidized glutathione (GSH and GSSG), vitamins A and E, total antioxidant status (TAS), glutathione peroxidase (GSH-Px) and reductase (GSH-Red) erythrocyte activities were compared between 43 NASH patients and 33 healthy controls. 4-HNE, GSH-Px, GSH-Red and TAS were evaluated by spectrophotometry, 8-OHdG by ELISA assay, GSH and GSSG by fluorimetric assay and vitamins A and E by high performance liquid chromatography. Dietary habits were also evaluated in these patients.


RESULTS
GSH levels (21.1 +/- 18.3 versus 33.1 +/- 22.2 microM, p = 0.01) and GSH/GSSG ratio (0.9 +/- 0.7 versus 1.5 +/- 0.8, p = 0.01) were lower and TAS (832 +/- 146 versus 630 +/-140 microM, p < 0.001) and vitamin E (47.1 +/- 14.9 versus 34.5 +/- 7.3 microM, p < 0.001) were higher in NASH patients, although there was no difference in GSH-Px and GSH-Red activities, 8-OHdG and 4-HNE levels between groups. After adjusting for total energy consumption, a negative correlation was found with total and saturated fat intake and GSH/GSSG ratio, and a positive correlation with carbohydrates, fiber, monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), specifically N-3 PUFA, and vitamins E, C, selenium and folate.


CONCLUSIONS
Our data suggest an impaired glutathione metabolism towards an oxidant status in NASH patients, correlating with a higher intake of saturated fat and a lower intake of carbohydrates. Plasmatic concentrations of oxidative stress cellular markers did not translate to hepatic oxidative damage.
Machado
Maiana Verdelho
MV
Unidade de Nutrição e Metabolismo, Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Portugal.
Ravasco
Paula
P
Jesus
Lia
L
Marques-Vidal
Pedro
P
Oliveira
Catarina R
CR
Proença
Teresa
T
Baldeiras
Inês
I
Camilo
Maria Ermelinda
ME
Cortez-Pinto
Helena
H
D000328:Adult; D000368:Aged; D000447:Aldehydes / Q000097:blood; D004032:Diet; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D004912:Erythrocytes / Q000201:enzymology; D005234:Fatty Liver / Q000097:blood*; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood; D005980:Glutathione Reductase / Q000097:blood; D006151:Guanosine / Q000031:analogs & derivatives / Q000097:blood; D006801:Humans; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D014810:Vitamin E / Q000097:blood
D000447:Aldehydes; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D006151:Guanosine; D014810:Vitamin E; C046215:8-hydroxyguanosine; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; C027576:4-hydroxy-2-nonenal